Evidence map›Paper›PMID 26508510›Full record

SynthesisClinical infectious diseases : an official publication of the Infectious Diseases Society of America2016

Host Genetic Susceptibility to Enteric Viruses: A Systematic Review and Metaanalysis.

Anita Kambhampati, Daniel C Payne, Veronica Costantini, Benjamin A Lopman

Open access · bronzeAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 3 pooled it
8.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 3 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Birth Cohort Studies Assessing Norovirus Infection and Immunity in Young Children: A Review.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2019
    Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Anita KambhampatiDivision of Viral Diseases, National Center for Immunization and Respiratory Diseases, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Daniel C PayneDivision of Viral Diseases, National Center for Immunization and Respiratory Diseases, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Veronica CostantiniDivision of Viral Diseases, National Center for Immunization and Respiratory Diseases, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Benjamin A LopmanDivision of Viral Diseases, National Center for Immunization and Respiratory Diseases, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Centers for Disease Control and Prevention · USNational Center for Immunization and Respiratory Diseases · US

Funding

Intramural CDC HHS CC999999
6 · The paper itself

Abstract

backgroundNorovirus and rotavirus are prominent enteric viruses responsible for severe acute gastroenteritis disease burden around the world. Both viruses recognize and bind to histo-blood group antigens, which are expressed by the fucosyltransferase 2 (FUT2) gene. Individuals with a functional FUT2 gene are termed "secretors." FUT2 polymorphisms may influence viral binding patterns and, therefore, may influence host susceptibility to infection by these viruses.

methodsWe performed a systematic review of the published literature on this topic. Data were abstracted and compiled for descriptive analyses and metaanalyses. We estimated pooled odds ratios (ORs) for infection using random-effects models.

resultsWe found that secretors were 9.9 times (95% confidence interval [CI], 3.9-24.8) as likely to be infected with genogroup II.4 noroviruses and 2.2 times as likely to be infected with genogroup II non-4 noroviruses (95% CI, 1.2-4.2) compared with nonsecretors. Secretors were also 26.6 times more susceptible to infections from P[8]-type rotaviruses compared with nonsecretors (95% CI, 8.3-85.0).

conclusionsOur analyses indicate that host genetic susceptibility to norovirus and rotavirus infection may be strain specific. As strain distribution and the proportion of genetic phenotypes vary in different countries, future studies should focus on differences in susceptibility among various ethnicities. Knowledge of innate susceptibility to rotavirus and norovirus can lead to improved understanding of both vaccine performance and individual risk of disease.

Indexed as

Caliciviridae InfectionsGenetic Predisposition to DiseaseRotavirus InfectionsFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseHumansNorovirusRotavirusFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseFUT2histo-blood group antigennorovirusrotavirus

Identifiers

PMID26508510
PMCPMC4679673
OpenAlexW2215600545

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.